PULMONARY PHARMACOLOGY & THERAPEUTICS
·
2021
·
IF 3.41
Bo Zou,Yue Fu,Chaofan Cao,Dianzhu Pan,Wei Wang,Lingfei Kong
Allergic asthma is a common airway inflammatory disorder with increasing morbidity and mortality worldwide. Gentiopicroside (GPS) is a secoiridoid glycoside compound that exhibits anti-inflammatory property. However, the effect of GPS on allergic asthma has not been reported yet. In this study, we investigated the role of GPS in a mouse model of ovalbumin (OVA)-induced allergic asthma and explored its potential mechanism. Mice were sensitized with OVA and gavaged with 20, 40, or 80 mg/kg GPS. Administration of GPS decreased lung wet-to-dry weight ratio. Histological analysis of H&E and PAS staining showed that GPS treatment alleviated inflammatory cell infiltration and goblet cell hyperplasia in lung tissue of OVA-sensitized mice. Moreover, GPS inhibited the recruitment of inflammatory cells including total cells, macrophages, eosinophils , lymphocytes and neutrophils and the secretion of T helper type 2 (Th2) cytokines (interleukin (IL)-4, IL-5 and IL-13) in bronchoalveolar lavage fluid (BALF) of OVA-sensitized mice in a dose dependent manner. The levels of OVA-specific immunoglobulin E (IgE) and pro-inflammatory tumor necrosis factor (TNF)-α were also attenuated by GPS treatment. Interestingly, GPS upregulated the expression of silent information regulator 1 (SIRT1) while downregulated the expression of acetyl-nuclear factor kappa B (NF-κB) p65 in lung tissue of OVA-sensitized mice. Furthermore, treatment with an SIRT1 inhibitor (EX-527) partially abolished the inhibitory effect of GPS on OVA-induced airway inflammation, suggesting that the anti-inflammation of GPS might be achieved through regulating SIRT1/NF-κB p65 signaling pathway . These findings indicate that GPS might be a novel drug candidate in the treatment of allergic asthma.
研究领域:
免疫学
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药理学
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呼吸医学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
·
2025
·Vol. 29
·期 8
·e70566
·
IF 4.2
Ying‐jie Ren,Tian‐qi Sun,Yu Lu,Dan‐Li Liu,Rui Gao,Ting Li,Min Guo,Qing‐hua Liu,Hai‐long Wang,Min Pang
Chronic obstructive pulmonary disease (COPD) is a widespread lung disease marked by alveolar wall damage, leading to inflammation and fibrosis. Key risk factors include age, smoking, sex, and education, with smoking being the most crucial. These factors are globally consistent and linked with aging. Club cell secretory protein 16 (CC16), primarily secreted by non‐ciliated bronchial epithelial cells, is crucial for pulmonary health, offering anti‐inflammatory and antioxidant benefits. CC16 levels are notably reduced in COPD, suggesting its enhancement as a potential treatment. In this study, cellular senescence of BEAS‐2B cells was stimulated using cigarette smoke extract (CSE) and the function of recombinant human CC16 protein (rhCC16) in cellular senescence was assessed by detecting the levels of β‐galactosidase, p16, p21, ROS and the underlined mechanism was revealed by measuring mitochondrial biogenesis and metabolism. Additionally, COPD mice were prepared, and rhCC16's role on the cellular senescence of lung tissues was examined. Our findings showed that rhCC16 ameliorated cellular senescence in BEAS‐2B cells and lung tissues of COPD mice accompanied by lower levels of β‐galactosidase, p16, p21 and ROS. Mechanically, rhCC16 mitigated senescence via triggering PGC‐1α expression through the AMPK/SIRT1 pathway and fostering mitochondrial biogenesis and metabolism to reduce the levels of ROS. Furthermore, the results also indicated that rhCC16 exerted its effect via both integrin α4β1 and clathrin‐mediated endocytosis. Collectively, rhCC16 suppresses cellular senescence and ameliorates COPD‐like symptoms by activating the AMPK/Sirt1‐PGC‐1‐α‐TFAM pathway to foster mitochondrial function.
研究领域:
医学
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生物学
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呼吸系统疾病
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分子生物学
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DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2025
·
IF 4.7
Hongtao Duan,Rui Zhang,Aiminuer Asikaer,Liang Pan,Shui Wang,Kuilong Huang,Deshuai Lou,Yuanqiang Wang,Zhihua Lin,Yan Shen
Background & Aims: Acute pancreatitis (AP) is a life-threatening condition, and hypertriglyceridemia (HTG) is recognized as a factor exacerbating AP and impeding pancreatic regeneration. Nicotinamide mononucleotide (NMN), a precursor in the biosynthesis of nicotinamide adenine dinucleotide (NAD + ), is extensively utilized to restore NAD + levels. However, the impact of NMN on HTG-AP has not been previously addressed, which prompted our investigation into its effects and underlying mechanisms in this study. Methods & Results: Here, through bioinformatics analysis and in vivo experiments, we identified abnormalities in the thioredoxin system. In vitro studies revealed that NMN rescued oleic acid (OA)- and palmitic acid (PA)-induced mitochondrial dysfunction and cellular injury in pancreatic acinar cells by suppressing thioredoxin-interacting protein (TXNIP) through NAD + /sirtuin 1 (SIRT1) signaling. Repeated administration of NMN significantly ameliorated P407 and caerulein (CER)-induced pancreatic injury and dysfunction in mice. Consistently, NMN exhibited the potential to reduce inflammatory responses, lower serum lipid levels, and mitigate the accumulation of reactive oxygen species (ROS). More importantly, sustained NMN treatment inhibited the NOTCH pathway and promoted M2-type macrophage dominance during the pancreatic repair phase, influencing early or late macrophage polarization, which significantly enhanced inflammation resolution. As expected, in vitro models using mouse bone marrow-derived macrophage (BMDM), RAW 264.7, and THP-1 cells confirmed that NMN influences macrophage phenotype through the NOTCH pathway. Conclusions: Therefore, NMN ameliorates pancreatic acinar cell injury via NAD + /SIRT1-mediated TXNIP suppression and may influence macrophage polarization by inhibiting NOTCH activation, offering a novel therapeutic strategy for the treatment and repair of HTG-AP.
研究领域:
医学
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生物化学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
FOOD AND CHEMICAL TOXICOLOGY
·
2013
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IF 3.01
Hua-Zong Ying,Jia-Na Zang,Li-Li Deng,Zhi-Yuan Wang,Chen-huan Yu
Pentamethylquercetin (PMQ) is a natural quercetin derivative found in a variety of edible herb. Although PMQ has potential as anti-diabetic agent, there have been no reports on its anti-adipogenic effects in the obese animals. This study investigated whether PMQ attenuates high-fat diet (HFD)-induced adipogenesis in the epididymal fat tissues of mice and explored its underlying mechanisms. In comparison with HFD-fed mice, mice fed with PMQ showed significantly lower body weight gain, adipose tissue mass, and plasma levels of triglyceride, total cholesterol, low-density lipoprotein cholesterol, and glucose, but higher plasma levels of high-density lipoprotein cholesterol. PMQ significantly reversed the HFD-induced regulation of Sirt1/mTOR signaling genes (Sirt1, mTOR , 4EBP1, and S6K1), and key adipogenic genes (PPARγ, SREBP1, FAS, ATGL, HSL, and Perilipin) in the epididymal adipose tissues of obese mice. However, nicotinamide appeared to partly inhibit PMQ-mediated anti-adipogenic effects involved in this attenuation. These results suggested that PMQ inhibited visceral adipogenesis by suppressing the Sirt1-mediated mTOR and adipogenesis signaling cascades. It might be a potential candidate for the treatment of obesity.
研究领域:
药理学
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营养学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
·
2023
·
IF 5.4
Qianyan Gao,Guodong Li,Yue Zu,Yanjiao Xu,Congyi Wang,Dong Xiang,Wenxi He,Tianze Shang,Xinwei Cheng,Dong Liu,Chengliang Zhang
Ethnopharmacological relevance Ginseng ( Panax ginseng C. A. Mey) is a common traditional Chinese medicine used for anti-inflammation, treating colitis, type 2 diabetes, diarrhea, and recovering hepatobiliary function. Ginsenosides, the main active components isolated from ginseng, possess liver and gallbladder diseases therapeutic potential. Aims of the study Cholestatic liver injury (CLI) is a liver disease induced by intrahepatic accumulation of toxic bile acids and currently lacks clinically effective drugs. Our previous study found that ginsenosides alleviated CLI by activating sirtuin 1 (SIRT1), but the effective ingredients and the underlying mechanism have not been clarified. This study aimed to identify an effective ingredient with the most significant activation effect on SIRT1 from the five major monomer saponins of ginsenosides: Rb1, Rd, Rg1, 20s-Rg3, and Rc further explore its protective effects on CLI, and elaborate its underlying mechanism. Materials and methods Discovery Studio 3.0 was used to conduct molecular docking between monomer saponins and SIRT1, and further detect the influence of monomer saponins on SIRT1 activity in vitro. Finally, it was determined that Rg1 had the most significant stimulative effect on SIRT1, and the hepatoprotective activity of Rg1 in CLI was explored in vivo. Wild-type mice were intragastrically α-naphthylisothiocyanate (ANIT) to establish an experimental model of intrahepatic cholestasis and Rg1 intervention, and then liver injury and cholestasis related indexes were detected. In addition, Liver-specific SIRT1 gene knockout (SIRT1 -/- ) mice were administered with ANIT and/or Rg1 to further investigate the mechanism of action of Rg1. Results The results of molecular docking and in vitro experiments showed that all the five ginsenoside monomers could bind to the active site of SIRT1 and promote SIRT1 activity in HepG2 cells. Among them, Rg1 exhibited the most significant stimulation of SIRT1 activity in cholestasis. Besides, it could ameliorate ANIT-induced inflammation and oxidative stress in HepG2 cells. Therefore, we investigated the hepatoprotective effect and mechanism of Rg1 on CLI. Results showed that Rg1 reversed the ANIT-induced increase in biochemical parameters, improved liver pathological injury, and decreased liver lipid accumulation, reactive oxygen species and pro-inflammatory factor levels. Mechanistically, Rg1 induced SIRT1 expression, followed by promoted the activity of Nrf2 and suppressed the activation of NF-κB. Interestingly, the hepatoprotective effect of Rg1 was blocked in SIRT1 -/- mice. Conclusion Rg1 mitigated ANIT-induced CLI via upregulating SIRT1 expression, and our results suggested that Rg1 is a candidate compound for treating CLI.
研究领域:
药理学
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肝病学
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分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CELLULAR AND MOLECULAR LIFE SCIENCES
·
2024
·Vol. 81
·期 1
·1-17
·
IF 6.2
Li Long,Liu Huimin,Chai Quanyou,Wei Junyi,Qin Yuqiao,Yang Jingyao,Liu He,Qi Jia,Guo Chunling,Lu Zhaoyang
Vascular calcification is a complication that is frequently encountered in patients affected by atherosclerosis, diabetes, and chronic kidney disease (CKD), and that is characterized by the osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs). At present, there remains a pressing lack of any effective therapies that can treat this condition. The sodium-glucose transporter 2 (SGLT2) inhibitor dapagliflozin (DAPA) has shown beneficial effects in cardiovascular disease. The role of this inhibitor in the context of vascular calcification, however, remains largely uncharacterized. Our findings revealed that DAPA treatment was sufficient to alleviate in vitro and in vivo osteogenic transdifferentiation and vascular calcification. Interestingly, our study demonstrated that DAPA exerts its anti-calcification effects on VSMCs by directly targeting SGLT2, with the overexpression of SGLT2 being sufficient to attenuate these beneficial effects. DAPA was also able to limit the glucose levels and NAD + /NADH ratio in calcified VSMCs, upregulating sirtuin 1 (SIRT1) in a caloric restriction (CR)-dependent manner. The SIRT1-specific siRNA and the SIRT1 inhibitor EX527 attenuated the anti-calcification effects of DAPA treatment. DAPA was also to drive SIRT1-mediated deacetylation and consequent degradation of hypoxia-inducible factor-1α (HIF-1α). The use of cobalt chloride and proteasome inhibitor MG132 to preserve HIF-1α stability mitigated the anti-calcification activity of DAPA. These analyses revealed that the DAPA/SGLT2/SIRT1 axis may therefore represent a viable novel approach to treating vascular calcification, offering new insights into how SGLT2 inhibitors may help prevent and treat vascular calcification. Graphical abstract Dapagliflozin attenuated vascular smooth muscle cells osteogenic transdifferentiation and vascular calcification through the SIRT1-mediated deacetylation and degradation of HIF-1α in a manner dependent on caloric restriction.
研究领域:
心血管疾病
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糖尿病
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慢性肾病
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分子生物学
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药理学
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产品关联
DOI
PubMed
高影响因子
TOXICOLOGY AND APPLIED PHARMACOLOGY
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2023
·
IF 3.8
Yixin Sun,Danyang Guo,Saiding Yue,Mingyan Zhou,Dongxu Wang,Fengjiao Chen,Lingling Wang
Background Doxorubicin (DOX), a chemotherapeutic drug, could relieve the progressions of various diseases. However, its clinical application is limited due to its cardiotoxicity. This study aimed to investigate the effects of afzelin (a flavonol glycoside found in Houttuynia cordata ) on the cardiotoxicity induced by DOX. Methods In ex-vivo, H9C2 cells were incubated with 20, 40, or 80 μM afzelin for 12 h, followed by the treatment with 1 μM DOX for 12 h. In vivo, C57BL/6 J mice were intraperitoneally injected with 4 mg/kg/day DOX on days 1, 7, and 14. Meanwhile, starting from day 1, mice were intragastrically administrated with 5 mg/kg/day or 10 mg/kg/day afzelin for 20 days. The cardiac function of mice was evaluated by detecting hemodynamic parameters using the M-mode echocardiography. Results DOX decreased the cell survival rate, and elevated apoptotic rate, as well as induced the oxidative stress and mitochondrial dysfunction in H9C2 cells. All these changes were alleviated by afzelin treatment in a concentration-dependent manner. The results were further proven by the mitigation of cardiac injury in vivo, as evidenced by the elevation of fractional shortening, heart weight/tibia length, and the rate of the increase/decrease of left ventricular pressure in mice subjected to DOX-induced cardiotoxicity. Furthermore, afzelin upregulated the expression of p-AMP-activated protein kinase alpha (AMPKα) and sirtuin1 (SIRT1). Dorsomorphin (an AMPKα inhibitor) abrogated the anti-cardiotoxicity effects of afzelin in H9C2 cells induced by DOX. Conclusion Afzelin protected against DOX-induced cardiotoxicity by promoting the AMPKα/SIRT1 signaling pathway.
研究领域:
药理学
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心脏病学
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细胞生物学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
Heliyon
·
2023
·
IF 4
Lanxin Li,Yang Zhang,Zhengqian Chen,Ruyong Yao,Zhongqiu Xu,Can Xu,Fujie He,Haitao Pei,Cui Hao
Parkinson's disease (PD) is the second most common neurodegenerative disease in the world, which is distinguished by the loss of dopaminergic (DA) neurons in the substantia nigra and the formation of intraneuronal. Numerous studies showed that the damage and dysfunction of mitochondria may play key roles in DA neuronal loss. Thus, it is necessary to seek therapeutic measures for PD targeting mitochondrial function and biogenesis. In this study, through screening the purchased compound library, we found that marine derived vidarabine had significant neuroprotective effects against rotenone (ROT) induced SH-SY5Y cell injury. Further studies indicated that vidarabine pretreatment significantly protected ROT-treated SH-SY5Y cells from toxicity by preserving mitochondrial morphology, improving mitochondrial function, and reducing cell apoptosis. Vidarabine also reduced the oxidative stress and increased the expression levels of PGC-1α, NRF1, and TFAM proteins, which was accompanied by the increased mitochondrial biogenesis. However, the neuroprotective effects of vidarabine were counteracted in the presence of SIRT1-specific inhibitor Ex-527. Besides, vidarabine treatment attenuated the weight loss, alleviated the motor deficits and inhibited the neuronal injury in the MPTP induced mouse model. Thus, vidarabine may exert neuroprotective effects via a mechanism involving specific connections between the SIRT1-dependent mitochondrial biogenesis and its antioxidant capacity, suggesting that vidarabine has potential to be developed into a novel therapeutic agent for PD.
研究领域:
神经科学
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药理学
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细胞生物学
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神经退行性疾病
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DOI
PubMed
高影响因子
Cellular and Molecular Gastroenterology and Hepatology
·
2024
·
IF 7.1
Liang Wang,Jinsong Li,Mingshan Jiang,Yue Luo,Xiaoke Xu,Juan Li,Yang Pan,Hu Zhang,Zhi-Xiong Jim Xiao,Yang Wang
Background and Aims Dysfunction of the intestinal epithelial barrier comprising the junctional complex of tight junctions and adherent junctions leads to increased intestinal permeability, which is a major cause of uncontrolled inflammation related to Inflammatory Bowel Disease (IBD). The NAD + -dependent deacetylase SIRT1 is implicated in inflammation and the pathological process of IBD. We aimed to elucidate the protective role and underlying mechanism of SIRT1 in cell-cell junction and intestinal epithelial integrity. Methods The correlation of SIRT1 expression and human IBD was analyzed by GEO or immunohistochemical analyses. BK5.mSIRT1 transgenic mice and WT mice were given dextran sodium sulfate (DSS) and the manifestation of colitis-related phenotypes were analyzed. Intestinal permeability was measured by FITC-Dextran and cytokines expression was analyzed by QPCR. The expression of the cell junction-related proteins in DSS-treated or SIRT1-knockdown Caco2 or HCT116 cells was analyzed by Western blotting. The effects of Nicotinamide mononucleotide (NMN) in DSS-induced mice colitis were investigated. Correlations of the SIRT1-β-TrCP1-Snail1-Occludin/Claudin-1/E-cadherin pathway with human IBD samples were analyzed. Results Reduced SIRT1 expression is associated with human IBD specimens. SIRT1 transgenic mice exhibit much-reduced manifestations of DSS-induced colitis. the activation of SIRT1 by NMN bolsters intestinal epithelial barrier function and ameliorates DSS-induced colitis in mice. Mechanistically, DSS down-regulates SiRT1 expression, leading to destabilization of β-TrCP1 and upregulation of Snail1, accompanied by reduced expression of E-cadherin, Occludin, and Claudin-1, consequently resulting in increased epithelial permeability and inflammation. The deregulated SIRT1-β-TrCP1-Snail1-Occludin/Claudin-1/E-cadherin pathway correlates with human IBD. Conclusion SIRT1 is pivotal in maintaining the intestinal epithelial barrier integrity via modulation of the β-TrCP1-Snail1-E-cadhein/Occludin/Claudin-1 pathway.
研究领域:
胃肠病学
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免疫学
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分子生物学
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细胞生物学
✓ 已验证
DOI
PubMed
高影响因子
BRAIN RESEARCH BULLETIN
·
2024
·
IF 3.5
Zhijuan Cheng,Jianglong Tu,Kai Wang,Fang Li,Yuan He,Wei Wu
Cerebral ischemia-reperfusion (IR) is the main pathophysiological process after stroke and can seriously impair neurological function. Wogonin, a natural flavonoid extracted from the roots of Scutellaria baicalensis, has potent anti-inflammatory properties. In this study, we investigated the protective mechanism of wogonin against middle cerebral artery occlusion (MCAO) and oxygen-glucose deprivation/reoxygenation (OGD/R) model-induced cerebral IR injury through adenosine 5‘-monophosphate-activated protein kinase (AMPK)/sirtuin 1 (SIRT1)/NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome axis. Our results showed that wogonin (20 mg/kg, intraperitoneal injection) effectively reduced infarct size, attenuated brain edema, improved neurological deficits, and alleviated histopathological damage. In addition, wogonin reduced microglial cell activation and inflammatory factors, including tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), IL-6, and IL-10, in brain tissue and serum after cerebral IR injury. Wogonin also effectively activated the AMPK/SIRT1 signaling pathway and inhibited NLPR3 inflammasome-related molecules upregulation in cerebral IR injury as well as in OGD/R-stimulated HT-22 cells. Furthermore, inhibition of the AMPK/SIRT1 signaling pathway by Compound C, an AMPK inhibitor, significantly reversed the protective effect of wogonin on OGD/R-induced NLRP3 inflammasome. Meanwhile, the protective effect of wogonin against brain IR injury was also reversed in the presence of compound C. These results suggest that wogonin ameliorates cerebral IR injruy-induced inflammation by inhibiting NLRP3 inflammasome through the AMPK/SIRT1 signaling pathway.
研究领域:
神经科学
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药理学
·
炎症研究
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分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Journal of Functional Foods
·
2018
·
IF 3.47
Qiao Lin,Xiu-Ying Chen,Ji Zhang,Yong-Liang Yuan,Wen Zhao,Bo Wei
The mechanisms underlying beneficial actions of Rutin, a food derived-polyphenolic bioflavonoid, against myocardial ischemia-reperfusion (MI/R) injury were detected. We found that Rutin could significantly ameliorate infarct size and attenuate cardiac dysfunctionto in some extent. Additionally, Rutin could also improve variation of myocardial zymogram and up-regulate antioxidant systems in heart. The selective SIRT1 inhibitor, Ex-527, exacerbated MI/R injury as evidenced by further increased oxidative stress and infracted area in heart tissue. Importantly, Ex-527 abolished the cardioprotective effect of Rutin in MI/R rats. Docking analysis further demonstrated the vital role of SIRT1 on Rutin's cardioprotective effect. We found that activation of SIRT1/Nrf2 signaling induced by Rutin contributes to the reduced oxidative stress, along with decreased apoptosis of cardiomyocytes in heart tissue. Overall, our findings suggest that SIRT1/Nrf2 signaling pathway may be a potential therapeutic target for the treatment of oxidative stress and apoptosis related myocardial diseases.
研究领域:
心脏病学
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药理学
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分子生物学
✓ 已验证
产品关联
DOI
高影响因子
Evidence-based Complementary and Alternative Medicine
·
2021
·
IF 2.63
Fei Zheng,Hai Xue,Bi-Xiang Wang,Man-Yu Wu,Dong-Xia Chen,Hao Yue,Lian-Kui Wen,Yang He
Vitis amurensis Rupr. “Beibinghong” is abundant in anthocyanins, including malvidin (Mv), malvidin-3-glucoside (Mv3G), and malvidin-3,5-diglucoside (Mv35 G). Anthocyanins offer nutritional and pharmacological effects, but their stability is poor. Interaction of malvid anthocyanins with caffeic acid through ultrahigh pressure technology produces stable anthocyanin derivatives. This study aims to identify the structure of stable mallow-like anthocyanins and to determine the effect of these stable anthocyanins on human umbilical vein endothelial cells (HUVECs) with H2O2-induced oxidative damage and the signaling pathway involved. The products of malvid anthocyanins and caffeic acid bonding were identified and analyzed using ultra-high performance liquid chromatography-quadrupole-Orbitrap mass spectrometry (UPLC-Q-Orbitrap MS/MS). The bonding products were malvidin-3-O-guaiacol (Mv3C), malvidin-3-O-(6″-O-caffeoyl)-glucoside (Mv3CG), and malvidin-3-O-(6″-O-caffeoyl)-5-diglucoside (Mv3C5G). An oxidative stress injury model in HUVECs was established using H2O2 and treated with Mv, Mv3G, Mv35 G, Mv3C, Mv3CG, and Mv3C5G at different concentrations (10, 50, and 100 μmol/L). Results showed that the above compound concentrations can significantly increase cell proliferation rate and reduce intracellular reactive oxygen species at 100 μmol/L. The effects of the most active products Mv and Mv3C on the AMP-activated protein (AMPK)/silencing information regulator-1 (SIRT1) pathway were analyzed. Results showed that Mv and Mv3C significantly increased SOD activity in the cells and significantly upregulated the expression of SIRT1 mRNA, SIRT1, and p-AMPK protein. However, they did not significantly change the expression of AMPK protein. After the silent intervention of siRNA in SIRT1 gene expression, the upregulation of SIRT1 and p-AMPK protein by Mv and Mv3C was significantly inhibited. These results indicate that stabilization malvid anthocyanins exerts an antioxidant activity via the AMPK/SIRT1 signaling pathway.
研究领域:
药理学
·
生物化学
·
细胞生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
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